Bjørg E. Kilavik, Sébastien Roux, Adrián Ponce-Alvarez, Joachim Confais, Sonja Grün, and Alexa Riehle
The timing of the task is represented in the temporal structure of significant spike synchronization at the population level. By practice, the temporal structure of synchrony was shaped. Synchrony became stronger and more localized in time during late experimental sessions, in parallel with a behavioral improvement, whereas the firing rate in the same neurons mainly decreased.
The brain processes in parallel sensory, temporal, and contextual information, which has to be combined appropriately to organize a movement.
It is widely accepted that sensorimotor funcitons are based on activity modulations in neuronal networks distributed over various brain structures. (Wise, 1984; Tanji and Kurata 1989; Riehle, 2005).
The timing of modulation of synchrony and firing rate at the population level in motor cortex suggests that synchrony may be preferentially involved in early preparatory and cognitive processes, whereas rate modulation may rather control movement initiation and execution (Riehle et al., 2000; Grammont and Riehle, 2003).
Showing posts with label motor learning. Show all posts
Showing posts with label motor learning. Show all posts
Thursday, October 8, 2009
Monday, May 18, 2009
Homeostatic synapse-driven membrane plasticity in nucleus accumbens neurons
By Ishikawa,M.; Mu,P.; Moyer,J.T.; Wolf,J.A.; Quock,R.M.; Davies,N.M.; Hu,X.T.; Schluter,O.M.; Dong,Y.
Abstract:
- Homeostatic mechanisms balances the input-output/synapse-membrane interaction at nucleus accumbens neurons.
- Studies on nucleus accumbens (NAc) neurons revealed a novel form of synapse-to-membrane homeostatic regulation (hSMP), homeostatic synapse-driven membrane plasticity (hSMP).
- Through hSMP, NAc neurons adjusted their membrane excitability to functionally compensate for basal shifts in excitatory synaptic input.
- hSMP is triggered by synaptic NMDA receptors.
Introduction:- Homeostatic plasticity is an important cellular mechanism through which neurons use the neuroplasticity mechinery to maintain stable functional output in an ever-changing internal and external environment (Turrigiano and Nelson, 2004).
- The functional output of a neuron relies on dynamic integration of synaptic inputs and intrinsic membrane excitability.
- It has long been known that homeostatic plasticity can occur independently at either synapses (Turrigiano and Nelson, 2004) or the membrane excitability (Zhang and Linden, 2003).
Results:
- hSMP in NAc slice cultures: NAc mediam spiny neuron (MSNs) increased excitability in slice culture.
- NMDA receptor mediates hSMP. DCS (D-cycloserine).
- hSMP in acute brain slices.
- Synapse-specific hSMP.
- SK channels mediate the expression of hSMP.
- Implication of hSMP in cocaine -induced membrane adaptation.
Abstract:
- Homeostatic mechanisms balances the input-output/synapse-membrane interaction at nucleus accumbens neurons.
- Studies on nucleus accumbens (NAc) neurons revealed a novel form of synapse-to-membrane homeostatic regulation (hSMP), homeostatic synapse-driven membrane plasticity (hSMP).
- Through hSMP, NAc neurons adjusted their membrane excitability to functionally compensate for basal shifts in excitatory synaptic input.
- hSMP is triggered by synaptic NMDA receptors.
Introduction:- Homeostatic plasticity is an important cellular mechanism through which neurons use the neuroplasticity mechinery to maintain stable functional output in an ever-changing internal and external environment (Turrigiano and Nelson, 2004).
- The functional output of a neuron relies on dynamic integration of synaptic inputs and intrinsic membrane excitability.
- It has long been known that homeostatic plasticity can occur independently at either synapses (Turrigiano and Nelson, 2004) or the membrane excitability (Zhang and Linden, 2003).
Results:
- hSMP in NAc slice cultures: NAc mediam spiny neuron (MSNs) increased excitability in slice culture.
- NMDA receptor mediates hSMP. DCS (D-cycloserine).
- hSMP in acute brain slices.
- Synapse-specific hSMP.
- SK channels mediate the expression of hSMP.
- Implication of hSMP in cocaine -induced membrane adaptation.
Homeostatic and nonhomeostatic modulation of learning in human motor cortex
By Patric Jung and Ulf Ziemann
Introduction
- Motor learning is of crucial importance throughout life for acquisition of new skills and reaccquisition of formerly known but, attributable to brain lesion, lost skills (Sanes, 2003; Krakauer, 2006).
- There is now substantial evidence that many types of motor learning occur in the primary motor cortex (M1) and involve synaptic plasticity in the form of long-term potentiation (LTP) (Rioult-Pedotti et al., 2000; Monfils and Teskey, 2004).
Introduction
- Motor learning is of crucial importance throughout life for acquisition of new skills and reaccquisition of formerly known but, attributable to brain lesion, lost skills (Sanes, 2003; Krakauer, 2006).
- There is now substantial evidence that many types of motor learning occur in the primary motor cortex (M1) and involve synaptic plasticity in the form of long-term potentiation (LTP) (Rioult-Pedotti et al., 2000; Monfils and Teskey, 2004).
Neocortical mechanisms in motor learning
by Jerome N Sanes
- Incontrovertible evidence: Many neocortical regions, including the motor-related areas, exhibit plasticity and are likely to contribute to motor- skill learning.
Leaning mechanisms
- Candidate mechanisms include fundamental modification in neural-spiking properties, the formation of new intrinsic or extrinsic synaptic contacts, the long-term potentiation or long-term depression of network synapses, and changes in intracortical processing.
- LTP and LTD have been proposed as mechanisms for learning and memory functions throughout the brain, although definitive proof of the relationship between synaptic plasticity and learning often is lacking.
Sunday, May 17, 2009
Voltage-dependent switching of sensorymotor integration by a lobster central pattern generator
By Romuald Nargeot
- Repeated sensory nerve stimulation gradually and long-lastingly strengthened the bursting of the LP neuron to the detriment of sensory-elicited inactivation.
- This strengthening of pyloric-timed rhytmic activity as enhanced by experimental depolarization of the neuron.
- When the LP neuron was hyperpolarized, the same sensory stimulation paradigm now gradually increased the susceptibility of the pyloric-timed bursting of the network neuron to sensory-elicited inactivation.
- Modulation of depolarization-activated and hyperpolarization-activated ionic conductances that underlie the intrinsic bursting properties of the LP neuron may contribute via differential voltage-dependent recruitment and effects to the respective adaptive processes.
- Repeated sensory nerve stimulation gradually and long-lastingly strengthened the bursting of the LP neuron to the detriment of sensory-elicited inactivation.
- This strengthening of pyloric-timed rhytmic activity as enhanced by experimental depolarization of the neuron.
- When the LP neuron was hyperpolarized, the same sensory stimulation paradigm now gradually increased the susceptibility of the pyloric-timed bursting of the network neuron to sensory-elicited inactivation.
- Modulation of depolarization-activated and hyperpolarization-activated ionic conductances that underlie the intrinsic bursting properties of the LP neuron may contribute via differential voltage-dependent recruitment and effects to the respective adaptive processes.
Thursday, May 7, 2009
PLASTICITY OF THE SPINAL NEURAL CIRCUITRY AFTER INJURY
By V. Reggie Edgerton, Niranjala J.K. Tillakaratne, Allison J. Bigbee, Ray D. de Leon, and Roland R. Roy
- A high level of functional recovery can be achieved following a complete spinal cord injury (SCI).
- The level of recovery in motor function is defined by the level and types of motor training or experience following the injury (Edgerton et al. 2001a, Wernig et al. 1995).
- Insight into the mechanisms of recovery and motor learning depends on a basic understanding of
the neural control of motor functions in the uninjured compared to the injured nervous system.
AUTOMATICITY IN POSTURE AND LOCOMOTION: SOME BASIC NEUROBIOLOGICAL PRINCIPLES OF MOTOR CONTROL BEFORE AND AFTER SCI
- Evolutionary learning in shaping the mammalian neural systems that control posture and locomotion.
- The automaticity within the spinal cord becomes even more critical for the CPG circuitry to successfully process sensory inputs.
Supraspinal Control of Posture and Locomtion
- The specific control features of each of the descending spinal tracts in controlling locomotion are poorly understood.
Spinal Control of Posture and Locomotion
1) CPG
2) SENSORY INPUT
- We propose that the spinal cord processes and interprets proprioception in a manner similar to how our visual system processes information (pattern recognition?).
- At any instant, the spinal cord receives an ensemble of information from all receptors throughout the body that signals a proprioceptive "image" that represents time and space.
- The importance of the CPG is not simply its ability to generate repetitive cycles, but also to receive, interpret, and predict the appropriate sequences of actions during any part of the step cycle, i.e., "state-dependence."
- The injured spinal cord interprets sensory changes in load and speed
- SCI patients can voluntarily initiate locomotion
3) THE INJURED SPINAL CORD IS AN "ALTERED" SPINAL CORD
- The spinal cord processes input and generates motor output in a different manner as a result of injury-related adaptations.
- Spasticity is a sign of activity in the spinal circuitry
MOTOR OUTPUT IS ENHANCED BY REPETITIVE TRAINING
Chronic Motor Training Modulates Spinal Plasticity to Enhance Motor Output After SCI
- Experiments with spinal cats using chronic locomotor training paradigms sugget that the ability to learn and successfully perform a motor task is dependent on repetitive practice.
- The functional state of the cord is shaped by specific locomotor training regimes.
- Although the mechanisms underlying locomotor training-enhanced plasticity is not well understood, it is clear that the physiological state of the cord can be affected by activity-dependent processes that can influence its ability to learn and perform a specified motor behavior.
The Spinal Cord Can Respond to Novel, Acute Perturbation
- An example of an object placed in front of a spinal cat stepping on a treadmill, a learning and memory-type phenomenon may be taking place ("smartness" of the spinal cord).
- Spinal cord is "solving" problems in real time based on the continually changing state of incoming peripehral information to elicit a nearly constant behavior, even though the means to the endpoint differ.
- These studies imply that spinal learning can occur in a very short period of time, and a type of memory trace allows for quicker adaptation upon reexposure to a given perturbation (Liu et al., 2003).
- The underlying cellular mechanisms are unknown.
- Hippocampal learning-like phenomena can occur in the spinal cord, but largely unknown.
Biochemical and Phamacological Evidence for Spinal Cord Plasticity After Injury
- The functinally recovered spinal animals showed no evidence of regeneration of descending pathways (Joynes et al. 1999) or showed minimal changes in hindlimb skeletal muscle properties to account for the recoery characteristics, the functinal behavior exhibited by these animals must have been mediated by the plasticity in existing spinal pathways.
- This plasticity may occur at any of many spinal cord regions or cell types such as motoneurons, premotor pattern-generating neurons, and/or nonneuronal celly types.
- There could also be anatomically altered synaptic connections, increased active zones of synapses, altered sensitivities of neurotoransmitter receptors, or altered pruduction of neurotransmitters.
- Data showed a significant role for these neurotransmitter systems in facilitating locomotor activity and thus suggest that these agents might be useful for inducing locomotion in SCI animals.
- Administration of 5-HT, its precursor 5-HTP, or the 5-HT agonists are also effective in improving locomotion in cats (Barbeau & Rossignol 1990, 1991) and rats (Feraboli-Lohnherr et al. 1999, Kim et al. 2001).
- The mechanism is unknown.
- The improvement of motor recovery upon the administration of of strychnine or bicuculline may occur by facilitating neuronal excitation by blocking the abnormally high levels of general inhibition resulting from a complete SCI (de Leon et al. 1999b).
- Nontrained spinal rats have increased GABA synthetic enzyme GAD67 and glycine and GABAA receptors in the lumbar spinal cord, whereas step-trained spinal rats have near-normal levels (Edgerton et al. 2001a, Tillakaratne et al. 2000).
- Training spinal cats to weight-bear also appears to reduce GABA signaling in some spinal interneurons.
- The amount of these enzymes depends on the type of training.
- These finding suggest that the inability of stand-trained spinal animals to step is closely linked to an elevated level of inhibition of flexor motor pools.
- The elevated level of a GABAA receptor subunit returns toward nearly undetectable control levels after six weeks of step training.
- Plasticity of spinal circuit may also be mediated by activity-dependent induction of neurotrophins.
Effects of Electrical Stimulation on Locomotor Recovery After SCI
HUMAN SCI: A PERSPECTIVE
Treadmill Training and the Recovery of Walking Ability After SCI
Use of Pharmacological Therapies in Enhancing Walking after SCI
CONCLUSION
- Training to stand improves standing ability and training to step improves stepping ability.
- One of the biochemical consequences of a complete SCI is an upregulation of inhibitory neurotransmitter systems, and step training reverses this effect.
- Physiological and biochemical state of the spinal conrd will affect how it respond to any given therapeutic intervention.
- A high level of functional recovery can be achieved following a complete spinal cord injury (SCI).
- The level of recovery in motor function is defined by the level and types of motor training or experience following the injury (Edgerton et al. 2001a, Wernig et al. 1995).
- Insight into the mechanisms of recovery and motor learning depends on a basic understanding of
the neural control of motor functions in the uninjured compared to the injured nervous system.
AUTOMATICITY IN POSTURE AND LOCOMOTION: SOME BASIC NEUROBIOLOGICAL PRINCIPLES OF MOTOR CONTROL BEFORE AND AFTER SCI
- Evolutionary learning in shaping the mammalian neural systems that control posture and locomotion.
- The automaticity within the spinal cord becomes even more critical for the CPG circuitry to successfully process sensory inputs.
Supraspinal Control of Posture and Locomtion
- The specific control features of each of the descending spinal tracts in controlling locomotion are poorly understood.
Spinal Control of Posture and Locomotion
1) CPG
2) SENSORY INPUT
- We propose that the spinal cord processes and interprets proprioception in a manner similar to how our visual system processes information (pattern recognition?).
- At any instant, the spinal cord receives an ensemble of information from all receptors throughout the body that signals a proprioceptive "image" that represents time and space.
- The importance of the CPG is not simply its ability to generate repetitive cycles, but also to receive, interpret, and predict the appropriate sequences of actions during any part of the step cycle, i.e., "state-dependence."
- The injured spinal cord interprets sensory changes in load and speed
- SCI patients can voluntarily initiate locomotion
3) THE INJURED SPINAL CORD IS AN "ALTERED" SPINAL CORD
- The spinal cord processes input and generates motor output in a different manner as a result of injury-related adaptations.
- Spasticity is a sign of activity in the spinal circuitry
MOTOR OUTPUT IS ENHANCED BY REPETITIVE TRAINING
Chronic Motor Training Modulates Spinal Plasticity to Enhance Motor Output After SCI
- Experiments with spinal cats using chronic locomotor training paradigms sugget that the ability to learn and successfully perform a motor task is dependent on repetitive practice.
- The functional state of the cord is shaped by specific locomotor training regimes.
- Although the mechanisms underlying locomotor training-enhanced plasticity is not well understood, it is clear that the physiological state of the cord can be affected by activity-dependent processes that can influence its ability to learn and perform a specified motor behavior.
The Spinal Cord Can Respond to Novel, Acute Perturbation
- An example of an object placed in front of a spinal cat stepping on a treadmill, a learning and memory-type phenomenon may be taking place ("smartness" of the spinal cord).
- Spinal cord is "solving" problems in real time based on the continually changing state of incoming peripehral information to elicit a nearly constant behavior, even though the means to the endpoint differ.
- These studies imply that spinal learning can occur in a very short period of time, and a type of memory trace allows for quicker adaptation upon reexposure to a given perturbation (Liu et al., 2003).
- The underlying cellular mechanisms are unknown.
- Hippocampal learning-like phenomena can occur in the spinal cord, but largely unknown.
Biochemical and Phamacological Evidence for Spinal Cord Plasticity After Injury
- The functinally recovered spinal animals showed no evidence of regeneration of descending pathways (Joynes et al. 1999) or showed minimal changes in hindlimb skeletal muscle properties to account for the recoery characteristics, the functinal behavior exhibited by these animals must have been mediated by the plasticity in existing spinal pathways.
- This plasticity may occur at any of many spinal cord regions or cell types such as motoneurons, premotor pattern-generating neurons, and/or nonneuronal celly types.
- There could also be anatomically altered synaptic connections, increased active zones of synapses, altered sensitivities of neurotoransmitter receptors, or altered pruduction of neurotransmitters.
- Data showed a significant role for these neurotransmitter systems in facilitating locomotor activity and thus suggest that these agents might be useful for inducing locomotion in SCI animals.
- Administration of 5-HT, its precursor 5-HTP, or the 5-HT agonists are also effective in improving locomotion in cats (Barbeau & Rossignol 1990, 1991) and rats (Feraboli-Lohnherr et al. 1999, Kim et al. 2001).
- The mechanism is unknown.
- The improvement of motor recovery upon the administration of of strychnine or bicuculline may occur by facilitating neuronal excitation by blocking the abnormally high levels of general inhibition resulting from a complete SCI (de Leon et al. 1999b).
- Nontrained spinal rats have increased GABA synthetic enzyme GAD67 and glycine and GABAA receptors in the lumbar spinal cord, whereas step-trained spinal rats have near-normal levels (Edgerton et al. 2001a, Tillakaratne et al. 2000).
- Training spinal cats to weight-bear also appears to reduce GABA signaling in some spinal interneurons.
- The amount of these enzymes depends on the type of training.
- These finding suggest that the inability of stand-trained spinal animals to step is closely linked to an elevated level of inhibition of flexor motor pools.
- The elevated level of a GABAA receptor subunit returns toward nearly undetectable control levels after six weeks of step training.
- Plasticity of spinal circuit may also be mediated by activity-dependent induction of neurotrophins.
Effects of Electrical Stimulation on Locomotor Recovery After SCI
HUMAN SCI: A PERSPECTIVE
Treadmill Training and the Recovery of Walking Ability After SCI
Use of Pharmacological Therapies in Enhancing Walking after SCI
CONCLUSION
- Training to stand improves standing ability and training to step improves stepping ability.
- One of the biochemical consequences of a complete SCI is an upregulation of inhibitory neurotransmitter systems, and step training reverses this effect.
- Physiological and biochemical state of the spinal conrd will affect how it respond to any given therapeutic intervention.
Labels:
5-HT,
GABAA,
motor learning,
NMDA,
recovery,
spinal cord
Sunday, April 19, 2009
Synaptic Bombardment Modulates Muscarinic Effects in Forelimb Motor Cortex
Niraj S. Desai and Elisabeth C. Walcott
Continuous synaptic bombardment with a complex barrage of excitatory and inhibitory inputs alter many aspects of neuronal responsiveness (by depolarizing neurons, increasing membrane conductance, and introducing fluctuations). This study shows how it shapes neuromodulation of postsynaptic responses by examining muscarinic modulation of forelimb motor cortex, a brain area in which cholinergic stimulation is known to be necessary for modifications during motor skill learning. Using a dynamic clamp system to inject simulated conductances
into pyramidal neurons, they mimicked in vivo-like activity by introducing a random background of excitatory and
inhibitory inputs. The presence of such background conductances strongly attenuated most muscarinic neuromodulatory effects, with the notable exception that sustained firing responses to trains of inputs were well preserved. This may be important for promoting plasticity in vivo.
The Journal of Neuroscience, February 22, 2006 • 26(8):2215–2226
Similar thing may be happening in the slug's CPG in the sea water. Most of my experiments testing neuromodulation have been done in HiDi saline, which suppresses anonymous synaptic bombardment.
Continuous synaptic bombardment with a complex barrage of excitatory and inhibitory inputs alter many aspects of neuronal responsiveness (by depolarizing neurons, increasing membrane conductance, and introducing fluctuations). This study shows how it shapes neuromodulation of postsynaptic responses by examining muscarinic modulation of forelimb motor cortex, a brain area in which cholinergic stimulation is known to be necessary for modifications during motor skill learning. Using a dynamic clamp system to inject simulated conductances
into pyramidal neurons, they mimicked in vivo-like activity by introducing a random background of excitatory and
inhibitory inputs. The presence of such background conductances strongly attenuated most muscarinic neuromodulatory effects, with the notable exception that sustained firing responses to trains of inputs were well preserved. This may be important for promoting plasticity in vivo.
The Journal of Neuroscience, February 22, 2006 • 26(8):2215–2226
Similar thing may be happening in the slug's CPG in the sea water. Most of my experiments testing neuromodulation have been done in HiDi saline, which suppresses anonymous synaptic bombardment.
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